Aurora B Overexpression Causes Aneuploidy and p21Cip1 Repression during Tumor Development

Alejandra González-Loyola, Gonzalo Fernández-Miranda, Marianna Trakala, David Partida, Kumiko Samejima, Hiromi Ogawa, Marta Cañamero, Alba de Martino, Ángel Martínez-Ramírez, Guillermo de Cárcer, Ignacio Pérez de Castro., William C. Earnshaw, Marcos Malumbres*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Aurora kinase B, one of the three members of the mammalian Aurora kinase family, is the catalytic component of the chromosomal passenger complex, an essential regulator of chromosome segregation in mitosis. Aurora B is overexpressed in human tumors although whether this kinase may function as an oncogene in vivo is not established. Here, we report a new mouse model in which expression of the endogenous Aurkb locus can be induced in vitro and in vivo. Overexpression of Aurora B in cultured cells induces defective chromosome segregation and aneuploidy. Long-term overexpression of Aurora B in vivo results in aneuploidy and the development of multiple spontaneous tumors in adult mice, including a high incidence of lymphomas. Overexpression of Aurora B also results in a reduced DNA damage response and decreased levels of the p53 target p21Cip1 in vitro and in vivo, in line with an inverse correlation between Aurora B and p21Cip1 expression in human leukemias. Thus, overexpression of Aurora B may contribute to tumor formation not only by inducing chromosomal instability but also by suppressing the function of the cell cycle inhibitor p21Cip1.

Original languageEnglish
Pages (from-to)3566-3578
Number of pages13
JournalMolecular and Cellular Biology
Issue number20
Early online date3 Aug 2015
Publication statusE-pub ahead of print - 3 Aug 2015


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